Expression of HOXA11 in the mid-luteal endometrium from women with endometriosis-associated infertility

Szczepańska, Magdalena; Wirstlein, Przemysław; Skrzypczak, Jana; Jagodzińśki, Paweł P.

doi:10.1186/1477-7827-10-1

Cited by 75 publications

(65 citation statements)

References 45 publications

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“…To demonstrate the utility and reliability of the SNAIL1-CBR reporter in vivo , we measured tissue-specific bioluminescence intensity during both physiologic and pathologic EMT processes known to be SNAIL1-dependent. Placental development is a robust EMT process and SNAIL1 has been implicated in trophoblast differentiation and uterine invasion [22, 23]. At 7.5 days post coitus (dpc) when trophoblast EMT is high [24], uterine SNAIL1-CBR signal was 5 fold higher compared to the basal signal (Fig.…”

Section: Resultsmentioning

confidence: 99%

Transient SNAIL1 Expression Is Necessary for Metastatic Competence in Breast Cancer

et al. 2014

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SNAIL1 has been suggested to regulate breast cancer metastasis based on analyses of human breast tumor transcriptomes and experiments using cancer cell lines and xenografts. However, in vivo genetic experimental support for a role for SNAIL1 in breast cancer metastasis that develops in an immunocompetent tumor microenvironment has not been determined. To address this question, we created a genetic SNAIL1 model by coupling an endogenous SNAIL1 reporter with an inducible SNAIL1 transgene. Using multiple genetic models of breast cancer, we demonstrated that endogenous SNAIL1 expression was restricted to primary tumors that ultimately disseminate. SNAIL1 gene deletion either during the premalignant phase or after primary tumors have reached a palpable size blunted metastasis, indicating that late metastasis was the main driver of metastasis and that this was dependent on SNAIL1. Importantly, SNAIL1 expression during breast cancer metastasis was transient and forced transient, but not continuous, SNAIL1 expression in breast tumors was sufficient to increase metastasis.

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Section: Resultsmentioning

confidence: 99%

Transient SNAIL1 Expression Is Necessary for Metastatic Competence in Breast Cancer

et al. 2014

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“…The normal connecting piece and upper midpiece contain a small portion of cytoplasm with a few endoplasmic reticulum vesicles. The midpiece is the major site of water influx and cell volume regulation, and these vesicles are important when sperm face hypo-osmotic challenges 89. The cytoplasmic droplet is indeed, really important for sperm function given that spermatozoa without it were immotile due to a defective spermatogenesis 90.…”

Section: Main Factors Affecting Sperm Motilitymentioning

confidence: 99%

Major regulatory mechanisms involved in sperm motility

Pereira¹,

Sá²,

Barros³

et al. 2017

Asian J Androl

229

171

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The genetic bases and molecular mechanisms involved in the assembly and function of the flagellum components as well as in the regulation of the flagellar movement are not fully understood, especially in humans. There are several causes for sperm immotility, of which some can be avoided and corrected, whereas other are related to genetic defects and deserve full investigation to give a diagnosis to patients. This review was performed after an extensive literature search on the online databases PubMed, ScienceDirect, and Web of Science. Here, we review the involvement of regulatory pathways responsible for sperm motility, indicating possible causes for sperm immotility. These included the calcium pathway, the cAMP-dependent protein kinase pathway, the importance of kinases and phosphatases, the function of reactive oxygen species, and how the regulation of cell volume and osmolarity are also fundamental components. We then discuss main gene defects associated with specific morphological abnormalities. Finally, we slightly discuss some preventive and treatments approaches to avoid development of conditions that are associated with unspecified sperm immotility. We believe that in the near future, with the development of more powerful techniques, the genetic causes of sperm immotility and the regulatory mechanisms of sperm motility will be better understand, thus enabling to perform a full diagnosis and uncover new therapies.

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“…In women with endometriosis, Wu et al showed increased DNMT3A and DNMT3B mRNA in ectopic endometriotic epithelium (33). More recently Szczepanka described elevated DNMT3A mRNA expression in the eutopic endometrium from women with endometriosis, although the other DNMTs remained unchanged (56). In contrast, Van Kaam observed little change in DNMT3B in whole tissue explants (30).…”

Section: Discussionmentioning

confidence: 99%

Aberrant expression and localization of deoxyribonucleic acid methyltransferase 3B in endometriotic stromal cells

Dyson

Kakinuma

Pavone

et al. 2015

Fertility and Sterility

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Objective To define the expression and function of DNA methyltransferases (DNMTs) in response to decidualizing stimuli in endometriotic cells compared with healthy endometrial stroma. Design Basic science. Setting University research center. Patients Premenopausal women with or without endometriosis. Interventions Primary cultures of stromal cells from healthy endometrium (E-IUM) or endometriomas (E-OSIS) were subjected to in vitro decidualization (IVD) using 1 µM medroxyprogesterone acetate, 35 nM 17β-estradiol, and 0.05 mM 8-Br-cAMP. Main Outcome Measure(s) DNMT1, DNMT3A, and DNMT3B expression in E-IUM and E-OSIS were assessed by qRT-PCR and immunoblotting. DNMT3B recruitment to the promoters of steroidogenic factor 1 (SF-1) and estrogen receptor α (ESR1) was examined by chromatin immunoprecipitation Results IVD treatment reduced DNMT3B mRNA (74%) and protein levels (81%) only in E-IUM. DNMT1 and DNMT3A were unchanged in both cell types. Significantly more DNMT3B bound to the SF-1 promoter in E-IUM compared with E-OSIS, and IVD treatment reduced binding in E-IUM to levels similar to those in E-OSIS. DNMT3B enrichment across three ESR1 promoters was reduced in E-IUM after IVD, although the more distal promoter showed increased DNMT3B enrichment in E-OSIS after IVD. Conclusions The inability to downregulate DNMT3B expression in E-OSIS may contribute to an aberrant epigenetic fingerprint that misdirects gene expression in endometriosis and contributes to its altered response to steroid hormones.

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Expression of HOXA11 in the mid-luteal endometrium from women with endometriosis-associated infertility

Cited by 75 publications

References 45 publications

Transient SNAIL1 Expression Is Necessary for Metastatic Competence in Breast Cancer

Transient SNAIL1 Expression Is Necessary for Metastatic Competence in Breast Cancer

Major regulatory mechanisms involved in sperm motility

Aberrant expression and localization of deoxyribonucleic acid methyltransferase 3B in endometriotic stromal cells

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